The hypoxia of high altitude stimulates ventilation. If the resultant respiratory alkalosis inhibits the initial increase in ventilation, then with prevention of alkalosis, ventilation should rise immediately to a stable plateau. Four subjects inspired CO2 (3.77%) from ambient air in a hypobaric chamber (P sub B = 440-445 torr) during 100 hours at high altitude. Ventilation (for given oxygen uptakes at rest and during exercise) increased promptly and remained stable. Four control subjects exposed to high altitude without CO2 supplementation showed the expected progressive increases in ventilation with time. The hyperoxic CO2 ventilatory response curve shifted progressively to the left with time in the control subjects but not in those given supplemental CO2. The latter group also failed to increase the ventilatory response to isocapnic hypoxia. Thus, CO2 supplementation at high altitude prevented the so called 'ventilatory acclimatization' from occurring. Prevention of respiratory alkalosis at high altitude probably permitted maintenance of (H+) at some central nervous system locus, thus allowing an uninhibited hypoxic stimulation of ventilation.